Epstein-Barr virus LMP2A: regulating cellular ubiquitination processes for maintenance of viral latency?

被引：23

作者：

Portis, T ^{[1
]}

Ikeda, M ^{[1
]}

Longnecker, R ^{[1
]}

机构：

[1] Northwestern Univ, Dept Microbiol & Immunol, Feinberg Sch Med, Chicago, IL 60611 USA

来源：

TRENDS IN IMMUNOLOGY | 2004年 / 25卷 / 08期

关键词：

D O I：

10.1016/j.it.2004.05.009

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Epstein-Barr virus (EBV) is a potentially oncogenic herpesvirus that persists in the B lymphocytes of most individuals. LMP2A might function as a central mediator of viral latency, allowing for long-term survival of infected B cells by providing a surrogate B-cell receptor signal. Recent studies support a model in which LMP2A utilizes ubiquitin-dependent processes to modulate cellular signaling pathways, including the Wnt and Notch pathways. Whether these pathways are exploited by LMP2A to maintain cell survival or to regulate viral gene expression during viral latency remains to be determined. These processes must be further explored to identify the factors that contribute to the maintenance of viral latency and possibly the development of EBV-associated malignancies.

引用

页码：422 / 426

页数：5

共 53 条

[31] Mammalian numb proteins promote notch1 receptor ubiquitination and degradation of the notch1 intracellular domain [J].

McGill, MA ;

McGlade, CJ .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (25) :23196-23203

[32] INTEGRAL MEMBRANE-PROTEIN 2 OF EPSTEIN-BARR-VIRUS REGULATES REACTIVATION FROM LATENCY THROUGH DOMINANT-NEGATIVE EFFECTS ON PROTEIN-TYROSINE KINASES [J].

MILLER, CL ;

BURKHARDT, AL ;

LEE, JH ;

STEALEY, B ;

LONGNECKER, R ;

BOLEN, JB ;

KIEFF, E .

IMMUNITY, 1995, 2 (02) :155-166

[33] AN INTEGRAL MEMBRANE-PROTEIN (LMP2) BLOCKS REACTIVATION OF EPSTEIN-BARR-VIRUS FROM LATENCY FOLLOWING SURFACE-IMMUNOGLOBULIN CROSS-LINKING [J].

MILLER, CL ;

LEE, JH ;

KIEFF, E ;

LONGNECKER, R .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (02) :772-776

[34] EPSTEIN-BARR-VIRUS LATENT MEMBRANE PROTEIN-2A BLOCKS CALCIUM MOBILIZATION IN B-LYMPHOCYTES [J].

MILLER, CL ;

LONGNECKER, R ;

KIEFF, E .

JOURNAL OF VIROLOGY, 1993, 67 (06) :3087-3094

[35] Epstein-Barr virus latent membrane protein 2A activates β-catenin signaling in epithelial cells [J].

Morrison, JA ;

Klingelhutz, AJ ;

Raab-Traub, N .

JOURNAL OF VIROLOGY, 2003, 77 (22) :12276-12284

[36] Notch-induced E2A ubiquitination and degradation are controlled by MAP kinase activities [J].

Nie, L ;

Xu, M ;

Vladimirova, A ;

Sun, XH .

EMBO JOURNAL, 2003, 22 (21) :5780-5792

[37]

Polakis P, 2000, GENE DEV, V14, P1837

[38] Epstein-Barr Virus (EBV) LNW2A induces alterations in gene transcription similar to those observed in Reed-Sternberg cells of Hodgkin lymphoma [J].

Portis, T ;

Dyck, P ;

Longnecker, R .

BLOOD, 2003, 102 (12) :4166-4178

[39] Epstein-Barr virus LMP2A interferes with global transcription factor regulation when expressed during B-lymphocyte development [J].

Portis, T ;

Longnecker, R .

JOURNAL OF VIROLOGY, 2003, 77 (01) :105-114

[40] The LMP2a signalosome - A therapeutic target for Epstein-Barr virus latency and associated disease [J].

Portis, T ;

Cooper, L ;

Dennis, P ;

Longnecker, R .

FRONTIERS IN BIOSCIENCE-LANDMARK, 2002, 7 :D414-D426

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